Haldol im maximum dosage

The influence of renal impairment on the pharmacokinetics of haloperidol has not been evaluated. About one-third of a haloperidol dose is excreted in urine, mostly as metabolites. Less than 3% of administered haloperidol is eliminated unchanged in the urine. Haloperidol metabolites are not considered to make a significant contribution to its activity, although for the reduced metabolite of haloperidol, back-conversion to haloperidol cannot be fully ruled out. Even though impairment of renal function is not expected to affect haloperidol elimination to a clinically relevant extent, caution is advised in patients with renal impairment, and especially those with severe impairment, due to the long half-life of haloperidol and its reduced metabolite, and the possibility of accumulation (see section ).

The intravenous route is not FDA approved and is generally not recommended except when no other alternatives are available. Intravenous administration appears to be associated with a higher risk of QT prolongation and torsade de pointes (TdP) than other forms of administration. The manufacturer recommends ECG monitoring for QT prolongation and arrhythmias if IV administration is required. A dose in the range of 1 to 5 mg IV has been suggested, with the dose being repeated at 30 to 60 minute intervals, if needed. A maximum IV dose has not been established. The lowest effective dose should be used in conjunction with conversion to oral therapy as soon as possible.

Also does not lead to cardiorespiratory depression. Effective in calming patients with delirium. IV route is not FDA approved but supported by the Society of Critical Care Medicine guidelines [Crit Care Med 30: 119, 2002]. D-blocker, works within 10-20 minutes and lasts for several hours. Only causes hypotension in hypovolemic patients or those on beta-blockers. May be ideal for weaning mechanically ventilated patients [Crit Care Med 22: 433, 1994]. IV doses range from –2 to 5-10 to 10–20 mg for mild, moderate, and severe anxiety. Individual patients show significant variation in serum levels after a single dose, so if there is no response give a second, double-dose after 10 minutes. Do not give a third dose (switch agents). Extrapyramidal reactions are rare and are decreased in incidence when benzodiazepines are added [J Intensive Care Med 4: 201, 1989]. More feared adverse events include NMS and torsades – note that % of patients on Haldol will show QT prolongation [Am J Cardiol 81: 238, 1998], thus pre-existing QT interval is a contraindication. Haldol-associated QT prolongation may be exacerbated in the presence of class III antiarrhythmics, hypocalcemia and intracranial hypertension. Also, Haldol is a mild selective -antagonist. Its safety has been questioned in acute head injury, as animal studies suggest worsening of secondary brain injury by the central antidopaminergic effect – a recent animal study suggested that single or multiple low doses of risperidone and haloperidol may be innocuous to recovery after traumatic brain injury, but that chronic high-dose treatments are detrimental [Crit Care Med 35:919, 2007]. Lastly, Haldol may lower the seizure threshold (Andrews, citation needed).